Facial Eczema (FE):-

Facial Eczema (FE):-

Hepatogenous photosensitization

The photosensitizing substance is in all instances phylloerythrin, a normal end product of chlorophyll metabolism excreted in the bile.

 When biliary secretion is obstructed by hepatitis or biliary duct obstruction, phylloerythrin accumulates

in the body and may reach levels in the skin that make it sensitive to light.

Although hepatogenous photosensitization is more common in animals grazing green pasture, it can occur in animals fed

entirely on hay or other stored feeds.

One of the Plants containing hepatotoxins

o Pithomyces chartarum fungus on perennial ryegrass causing  

facial eczema by poisonous substance called "sporidesmin"

Facial Eczema (FE):-

Pithomycotoxicosis

Pathogenesis: -

The sporidesmins are excreted via the biliary system, in which they produce severe cholangitis and pericholangitis (biliary duct obstruction ) as a result of tissue necrosis which restricts excretion of bile pigments and results in jaundice. Similarly, failure to excrete phylloerythrin in bile leads phylloerythrin accumulatesin the body and may reach levels in the skin that make it sensitive to light (photosensitization).

Previous ingestion of toxic spores causes potentiation; thus, a succession of small intakes of the spores can lead to subsequent severe outbreaks.

N.B:- Phylloerythrin, a normal breakdown product of chlorophyll in the rumen, is normally absorbed into the portal bloodstream and excreted by the liver in the bile. With the bile ducts blocked, it accumulates and spills over into the blood stream.

Clinical Findings: -

 Few signs are apparent until photosensitization and jaundice appear ~10–14 days after intake of the toxins (( The first signs of ingestion of the sporidesmin toxin may be

an initial transient diarrhea and sudden milk production drop and Animals frantically seek shade. Even short exposure to the sun rapidly produces the typical erythema and edema of photodermatitis in nonpigmented skin.))

·     Exposed hairless and non-pigmented skin such as on the face, ears, lips,

vulva, udder and teats, and inside the hind legs becomes reddened, raised and edematous. The nictating membrane (third eyelid) commonly appears sunburnt. Cows may be restless, seek shade and lick or rub affected areas and if photosensitization is acute, collapse showing extreme pain.

Skin lesions may progress further and eventually lead to large sheets of skin peeling off, especially in Holstein-Friesian cows.

·     In severe cases, cystitis (inflammation of the bladder) may also occur, with affected cows exhibiting prolonged and frequent urination.

·      Hemoglobinuria and jaundice may also occur, associated with an acute hemolytic crisis, often as a prelude to a severe outbreak of FE . However, they are not seen in many herd outbreaks.


As already stated, most animals affected by FE do not show obvious signs, but will have some degree of liver damage and their overall well-being and milk production will be affected. For every cow in a herd with skin lesions,

up to 10 or more cows may be affected sub-clinically. A New Zealand study of 565,000 dairy cows (Faull, 1991) showed that only 6% of all animals had skin lesions, while 38% had liver damage.

In affected animals a drop in milk production may be temporary, but in severe cases affected cows may dry off completely. Cows that die in the short term generally do so from complications of photosensitivity rather than liver

failure. A small number of affected animals may apparently

recover, only to go down and die around the time of calving, the damaged liver being unable to handle the additional stress around the time of calving.

Prognosis:-

Mortality may not be very high, especially when FE affected animals are given shelter and adequate care.

Cows have a remarkable ability to regenerate liver compared to sheep.

Key points

? FE is not a skin disease. The skin condition seen with FE is the result of

   the liver damage caused by the sporidesmin toxin.

? It is very common to have a significant FE problem without animals

   showing photosensitisation.

 It is the 80% of cows without skin lesions, with liver damage,

  that give the major economic impact.

? FE doesn’t just occur on white skin.

  Even black cattlget FE (Every animal has a liver).

? Zinc can only help prevent FE. It cannot reverse liver

damage already done by sporidesmin.



I have came across this many time over my career, My advice I give to people to deal with this problem is the early the better you detect the better the result for the infected animal. You must always treat with vitamins to help keep the liver function properly due to the toxins being released by the fungus. Treat with anti inflammatory Cover them in engine sump oil which will also help with keeping the outer layer moist and help prevent cracking of the skin then resulting in secondary infections then put them in a dark area to lesson the effects of the uv light. The important lesson I learned with problems like this is good records on health trends, for example we had a location on the property it was a small area about 1 hectare in size and in spring if we grazed in this location or cut fodder we would get 1 in 50 head with this problem.

Karen Mc Bride

Mastitis Detector at Australian Dairy Farmers

4 年

Vitamin A+D+E Injection!

要查看或添加评论,请登录

社区洞察

其他会员也浏览了